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At least 1,477 records · Page 82Linked to original sources
PubMed1981

A new beta 2-adrenoceptor agonist with alpha 1-adrenoceptor blocking properties.

The phenylethanolamine D2343 exhibits a dualistic adrenoceptormediated effect, i.e, a beta-agonistic effect combined with an alpha-antagonistic one. Tracheal smooth muscles and heart preparations were used to gauge the agonistic effect of adrenergic beta-receptors. Rabbit aorta and rat vas deferens were used to determine the alpha-adrenoceptor blocking activity. The beta-adrenoceptor activity of D2343 was classified as beta 2-type with about the same efficacy as the beta 2-selective terbutaline on tracheal muscle. The effect on isolated heart preparations was greater than that produced by terbutaline. The alpha-receptor blocking capacity was directed against the alpha 1-receptor type and was of nearly the same potency as for phentolamine.

Adrenergic alpha-Antagonists↗
PubMed1984

Selectivity of beta-adrenergic stimulating and blocking agents.

Studies have been performed to answer two questions: whether there are subgroups of beta 2-receptors separating effects in bronchial and skeletal muscle and whether beta 1-receptors in asthmatic airways mediate bronchoconstriction. Asthmatic patients have been studied in randomised cross-over trials. Effects on FEV1, heart rate and skeletal muscle tremor have been monitored. In some experimental studies, two new compounds, D2343 and QH-25, have shown a selectivity for beta 2-receptors in bronchial muscle compared to skeletal muscle. Studies in asthmatics did not confirm this. Thus, the beta 2-receptors in the two organs appear to be identical. The clinical effect of beta 1-receptors in the the airways was studied by giving selective beta 1-receptor blocking agents. It was shown that pafenolol , a beta-blocker more beta 1-selective than metoprolol, had less effect on FEV1 than metoprolol given in equipotent beta 1-blocking doses. Beta 1-receptor stimulation with a new selective beta 1-stimulating agent, prenalterol, did not give bronchodilation in doses which gave a significant increase of heart rate. Thus, beta 1-receptors do not contribute to bronchodilation in asthmatic patients.

Adrenergic beta-Agonists↗
PubMed1984

Evidence for neuronal uptake and release of norfenefrine and evaluation of its alpha-agonistic effects in the rabbit pulmonary artery.

Rabbit pulmonary artery strips were used for the evaluation of the alpha 1-/alpha 2-agonistic activity of norfenefrine (active principle of the antihypotensive agent Novadral) and for the investigation of neuronal uptake and release mechanisms for norfenefrine in the vessel wall. At 0.1 and 1 mumol/l, norfenefrine caused contractions of the artery strips, while presynaptic inhibition of stimulation-evoked noradrenaline release could not be detected with certainty. Thus, in the range tested, alpha 1-agonistic activity was more pronounced. Uptake and release of 3H-norfenefrine was studied on noradrenaline-depleted arteries. Rabbits were pretreated either with alpha-methyl-p-tyrosine (metirosine, alpha-MT) to inhibit noradrenaline synthesis without affecting storage vesicle function or with reserpine to eliminate vesicular storage capacity. In arteries from animals pretreated with alpha-MT, more substance was retained after preincubation with 3H-norfenefrine, in comparison with reserpine pretreated arteries, and about 2% of the substance was released from Arteries from reserpine pretreated animals retained less 3H-norfenefrine after preincubation, in comparison with alpha-MT pretreated arteries, and less than 0.2% was released per stimulation period. After alpha-MT treatment, tension developed upon stimulation was enhanced after norfenefrine preincubation, while contractions of reserpine pretreated arteries were independent of norfenefrine preincubation. These results provide evidence for an uptake of norfenefrine in the noradrenaline storage vesiculation period. After alpha-MT treatment, tension developed upon stimulation was enhanced after norfenefrine preincubation, while contractions of reserpine pretreated arteries were independent of norfenefrine preincubation. These results provide evidence for an uptake of norfenefrine in the noradrenaline storage vesicles and a vesicular co-secretion of norfenefrine with noradrenaline upon stimulation. The impaired sympathetic transmission was thereby improved.

2-Hydroxyphenethylamine↗
PubMed1982

The role of cyclic AMP in the regulation of exocytosis in the rat parotid gland: evidence obtained with the isoproterenol analog PI-39.

The isoproterenol analog, PI-39, induced a dose-dependent release of alpha-amylase from rat parotid minces in vitro. This effect was blocked by propranolol, a beta-adrenergic antagonist. PI-39 alone had no effect on parotid cyclic AMP levels or on protein kinase activation as assessed by the activity ratios method. However, PI-39 produced a dose-dependent increase in these parameters when a phosphodiesterase inhibitor was added to tissue minces simultaneously with the isoproterenol analog. Both isoproterenol and PI-39 altered the phosphorylation state of at least three specific endogenous phosphoproteins in (32P)-Pi prelabelled minces. The presence of a phosphodiesterase inhibitor was not required to demonstrate the effects of PI-39 on protein phosphorylation. Studies of endogenous protein phosphorylation in parotid broken cell preparations demonstrated that the phosphorylation of at least two of the PI-39 and isoproterenol-affected phosphoproteins are influenced by cyclic AMP. This study demonstrates that, under certain conditions, it is possible to activate a cyclic AMP-regulated biological process without elevating the total cellular cyclic AMP concentration or the protein kinase activity ratio.

Amylases↗